medigraphic.com

2019, Número 1

<< Anterior Siguiente >>

Rev Clin Esc Med 2019; 9 (1)


Cardiomiopatía diabética: entidad poco conocida y el impacto terapéutico de los inhibidores del cotransporrtador sodio-glucosa tipo 2 en el miocardio diabetico

Navarro SJ, Vinocour FM

Idioma: Español
Referencias bibliográficas: 45
Paginas: 11-27
Archivo PDF: 409.42 Kb.


RESUMEN

La cardiomiopatía diabética es una entidad que se origina a partir de una complicación microvascular de la diabetes mellitus tipo 2, la cual se desarrolla por la sinergia de varios elementos metabólicos generados por la hiperglicemia crónica y oxidación ácidos grasos libres que causan un impacto perjudicial por diferentes vías bioquímicas a nivel del miocardio provocando cambios estructurales y funcionales, como consecuencia generan disfunción diastólica y sistólica temprana antes de producir síntomas asociados. Debido a lo anterior es de suma importancia entender esta patología desde el plano fisiopatológico, por otra parte, establecer un diagnóstico oportuno por métodos establecidos como el ecocardiograma y posibles tratamientos en la actualidad para la mejoría de la contractibilidad miocárdica. En el presente artículo se revisan los mecanismos fisiopatológicos en base a los procesos metabólicos en la diabetes mellitus que afectan el miocardio generando una disminicion en la eficiencia cardiaca por ende provocando una insuficiencia cardiaca a largo plazo, también se analizara los métodos diagnósticos más precisos y concluyentes para establecer la cardiomiopatía diabética. Por otro lado, se analizarán los efectos terapéuticos de los medicamentos inhibidores del cotransportador sodio-glucosa tipo 2 en el miocardio en base sus efectos beneficios ya demostrados y a la vez en teorías e hipótesis que se han planteado a partir de investigaciones experimentales y observacionales.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Acar E, Ural D, Bildirici U, Şahin T, Yılmaz I. Diabetic cardiomyopathy. Anadolu Kardiyol Derg 2011; 11: 732-7.

  2. Aneja A, Tang WH, Bansilal S, Garcia M. Diabetic Cardiomyopathy: Insights into Pathogenesis, Diagnostic Challenges, and Therapeutic Options. Am J Med. 2008; 121:748-57.

  3. Brahma M, Pepin M, Wende A. My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy. Diabetes Metab J. 2017; 41: 1–9.

  4. Niemann B, Rohrbach S, Miller MR, Newby DE, Fuster V, Kovacic JC. Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution Part 3 of a 3-Part Series. J Am Coll Cardiol 2017; 70:230–51.

  5. Paneni F, Beckman J, Creager M. Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I. Eur Heart J. 2013; 34:2436-43.

  6. Jia G, Whaley-Connell A, Sowers A. Diabetic cardiomyopathy: a hyperglycaemia and insulin-resistanceinduced heart disease. Diabetologia. 2018; 61:21-28.

  7. Jia G, Hill MA, Sowers JR. Diabetic Cardiomyopathy An Update of Mechanims Contributing to This Clinical Entity. Circ Res. 2018; 122:624-638.

  8. Shah M, Brownlee M. Molecular and Cellular Mechanisms of Cardiovascular Disorders in Diabetes. Circ Res. 2016; 118:1808-29.

  9. Gilca GE, Stefanescu G, Badulescu O, Tanase DM, Bararu I, Ciocoiu M. Diabetic Cardiomyopathy: Current Approach and Potential Diagnostic and therapeutic Targets. J Diabetes Res. 2017; 2017:1310265.

  10. Wang C, Hess C, Hiatt W, Goldfine A. Clinical Update: Cardiovascular Disease in Diabetes Mellitus Atherosclerotic Cardiovascular Disease and Heart Failure in Type 2 Diabetes Mellitus – Mechanisms, Management, and Clinical Considerations. Circulation. 2016; 133:2459–2502.

  11. Hu X, Bai T, Xu Z, Liu Q, Zheng Y, Cai L. Pathophysiological Fundamentals of Diabetic Cardiomyopathy. Compr Physiol. 2017; 7:693-711.

  12. Liu Q, Wang S, Cai L. Diabetic cardiomyopathy and its mechanisms: Role of oxidative stress and damage. J Diabetes Invest 2014; 5: 623–634.

  13. Negishi K. Echocardiographic feature of diabetic cardiomyopathy: where are we now? Cardiovasc Diagn Ther. 2018; 8:47-56.

  14. Kovács A, Oláh A, Lux A, et al. Strain and strain rate by speckle-tracking echocardiography correlate with pressure-volume loop-derived contractility indices in a rat model of athlete’s heart. Am J Physiol Heart Circ Physiol. 2015; 308:H743-8.

  15. Loncarevic B, Trifunovic D, Soldatovic I, Vujisic- Tesic B. Silent diabetic cardiomyopathy in everyday practice: a clinical and echocardiographic study. BMC Cardiovasc Disord. 2016; 16:242.

  16. Yang H, Wang Y, Negishi K, Nolan M, Marwick T. Pathophysiological effects of different risk factors for heart failure. Open Heart. 2016; 3(1): e000339.

  17. Aronsen JM, Swift F, Sejersted OM. Cardiac sodium transport and excitation–contraction coupling. J Mol Cell Cardiol. 2013; 61:11-9.

  18. Despa S, Bers D. Na+ transport in the normal and failing heart — Remember the balance. J Mol Cell Cardiol. 2013; 61:2-10.

  19. Lambert R, Srodulski S, Peng X, Margulies K, Despa F, Despa S. Intracellular Na+ Concentration ([Na+] i) Is Elevated in Diabetic Hearts Due to Enhanced Na+–Glucose Cotransport. J Am Heart Assoc. 2015; 4(9): e002183.

  20. Bertero E, Roma L, Ameri P, Maack C. Cardiac effects of SGLT2 inhibitors: the sodium Hypothesis. Cardiovasc Res. 2018; 114:12-18.

  21. Zinman B, Wanner C, Lachin J, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes. N Engl J Med 2015; 373:2117-28.

  22. Neal B, Perkovic V, Mahaffey K, et al. Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes. N Engl J Med 2017; 377:644-657.

  23. Cefalu W, Bakris G, Blonde L, et al. Standards of Medical Care in Diabetes. Diabetes Care. 2017; 40: S4-S5.

  24. Hattersley A, Thorens B. Type 2 Diabetes, SGLT2 Inhibitors, and Glucose Secretion. N Engl J Med. 2015; 373:974-6.

  25. Staels B. Cardiovascular Protection by Sodium Glucose Cotransporter 2 Inhibitors: Potential Mechanisms. Am J Med. 2017; 130: S30-S39.

  26. Marx N, McGuire D. Sodium-glucose cotransporter-2 inhibition for the reduction of cardiovascular events in high-risk patients with diabetes mellitus. Eur Heart J. 2016; 37:3192-3200.

  27. Heerspink H, Perkins B, Fitchett D, Husain M, Cherney D. Sodium Glucose Cotransporter 2 Inhibitors in the Treatment of Diabetes Mellitus: Cardiovascular and Kidney Effects, Potential Mechanisms, and Clinical Applications.Circulation. 2016; 134:752-72.

  28. Taylor S, Blau J, Rother K. SGLT2 Inhibitors May Predispose to Ketoacidosis. J Clin Endocrinol Metab. 2015; 100:2849-52.

  29. Packer M, Anker S, Butler J, Filippatos G, Zannad F. Effects of Sodium-Glucose Cotransporter 2 Inhibitors for the Treatment of PatientsWith Heart Failure Proposal of a Novel Mechanism of Action. JAMA Cardiol. 2017; 2:1025-1029.

  30. Karg MV, Bosch A, Kannenkeril D, et al. SGLT-2- inhibition with dapagliflozin reduces tissue sodium content: a randomised controlled trial. Cardiovasc Diabetol. 2018; 17:5.

  31. Baker WL, Buckley LF, Kelly MS, et al. Effects of Sodium-Glucose Cotransporter 2 Inhibitors on 24-Hour Ambulatory Blood Pressure: A Systematic Review and Meta-Analysis. J Am Heart Assoc. 2017; 6: e005686.

  32. Kimura G. Diuretic Action of Sodium-Glucose Cotransporter 2 Inhibitors and Its Importance in the Management of Heart Failure. Circ J. 2016; 80:2277-2281.

  33. McMurray J. EMPA-REG: the “diuretic hypothesis.” J Diabetes Complications 2016; 30:3–4.

  34. Kaplan A, Abidi E, El-Yazbi A, Eid A, Booz GW, Zouein FA. Direct cardiovascular impact of SGLT2 inhibitors: mechanisms and effects. Heart Fail Rev. 2018 May;23(3):419-437.

  35. Abdul-Ghani M, Del Prato S, Chilton R, DeFronzo R. SGLT2 Inhibitors and Cardiovascular Risk: Lessons Learned From the EMPA-REG OUTCOME Study. Diabetes Care 2016; 39:717–725.

  36. Lee TM, Changd NC, Lin SZ. Dapagliflozin, a selective SGLT2 Inhibitor, attenuated cardiac fibrosis by regulating the macrophage polarization via STAT3 signaling in infarcted rat hearts. Free Radic Biol Med. 2017; 104:298-310.

  37. Lopaschuk G, Verma S. Empagliflozin’s Fuel Hypothesis: Not so Soon. Cell Metab. 2016; 24:200-2.

  38. Mudaliar S, Alloju S, Henry R. Can a Shift in Fuel Energetics Explain the Beneficial Cardiorenal Outcomes in the EMPA-REG OUTCOME Study? A Unifying Hypothesis. Diabetes Care 2016; 39:1115– 1122.

  39. Heart Relies on Ketone Bodies as a Fuel. Circulation. 2016; 133:698-705.

  40. Baartscheer A, Schumacher C, Wüst R, et al. Empagliflozin decreases myocardial cytoplasmic Na+ through inhibition of the cardiac Na+/H+ exchanger in rats and rabbits. Diabetologia (2017) 60:568–573.

  41. Bertero E, Roma LP, Ameri P, Maack C. Cardiac effects of SGLT2 inhibitors: the sodium hypothesis. Cardiovasc Res. 2018; 114:12-18.

  42. Packer M. Role of the Sodium-Hydrogen Exchanger in Mediating the Renal Effects of Drugs Commonly Used in the Treatment of Type 2 Diabetes. Diabetes Obes Metab. 2018; 20:800-811.

  43. Packer M. Activation and Inhibition of Sodium- Hydrogen Exchanger Is a Mechanism That Links the Pathophysiology and Treatment of Diabetes Mellitus with That of Heart Failure. Circulation. 2017; 136:1548–1559.

  44. Uthman L, Baartscheer A, Bleijlevens B, et al. Class effects of SGLT2 inhibitors in mouse cardiomyocytes and hearts: inhibition of Na+/H+ exchanger, lowering of cytosolic Na+ and vasodilation. Diabetologia. 2017; 61:722-726.

  45. Ferrannini E, Mark M, Mayoux E. CV Protection in the EMPA-REGOUTCOME Trial: A "Thrifty Substrate Hypothesis. Diabetes Care 2016; 39:1108–111.




2020     |     www.medigraphic.com